Feline immunodeficiency virus infection

Abstract

Feline immunodeficiency virus (FIV) (formerly feline T-lymphotropic lentivirus or FTLV) was first isolated from a group of cats in Petaluma, California in 1986. The virus is a typical lentivirus in gross and structural morphology. It replicates preferentially but not exclusively in feline T-lymphoblastoid cells, where it causes a characteristic cytopathic effect. The major structural proteins are 10, 17 (small gag), 28 (major core), 31 (endonuclease?), 41 (transmembrane?), 52 (core precursor polyprotein), 54 62 (reverse transcriptase?), and 110 130 (major envelope) kilodaltons in size. The various proteins are antigenically distinguishable from those of other lentiviruses, although serum from EIAV-infected horses will cross-react with some FIV antigens. Kittens experimentally infected with FIV manifest a transient (several days to 2 weeks) fever and neutropenia beginning 4 to 8 weeks after inoculation. This is associated with a generalized lymphadenopathy that persists for up to 9 months. Most cats recover from this initial phase of the disease and become lifelong carriers of the virus. Complete recovery does not occur to any extent in nature or in the laboratory setting. One experimentally infected cat died from a myeloproliferative disorder several months after infection. The terminal AIDS-like phase of the illness has been seen mainly in naturally infected cats. It appears a year or more following the initial infection in an unknown proportion of infected animals. FIV has been identified in cats from all parts of the world. It is most prevalent in high density populations of free roaming cats (feral and pet), and is very uncommon in closed purebred catteries. Male cats are twice as likely to become infected as females. Older male cats adopted as feral or stray animals are at the highest risk of infection, therefore. The infection rate among freely roaming cats rises throughout life, and reaches levels ranging from less than 1% to 12% or more depending on the area. Clinically affected cats tend to be 5 years or older at the time of hospitalization. Experimental and seroepidemiologic studies suggest that FIV is transmitted mainly by bites. Intimate, non-traumatic contact (mutual grooming, shared use of food, water and litter pans) is inefficient in transmitting the infection. In utero and venereal transmission could not be demonstrated in laboratory settings. There is no statistical linkage between FIV and feline leukemia virus (FeLV) infections in nature. The FeLV infection rate in FIV-infected animals is the same as it is for non-FIV-infected cats. Cats with both infections tend to die more quickly and at a younger age than animals infected with FIV alone. There is a statistical linkage between FIV infection and infection with a third retrovirus of cats, feline syncytium-forming virus (FeSFV). This is probably due to the common mode of transmission of these two retroviruses. The clinical manifestations of terminal FIV infection in nature are varied. One group of cats succumbs over a period of months or years to progressive secondary or opportunistic infections of the oral cavity, upper respiratory tract, gastrointestinal tract, skin, or urinary tract. Others suffer from vague signs of illness, unexplainable anemias, FeLV negative myeloproliferative or lymphoproliferative neoplasms, or neurologic disorders. Neurologic signs are usually of a cortical nature, with dementia and behavioral abnormalities predominating. Similarities between FIV infection of cats and HIV infection of man are striking, making FIV infection of cats a good model for human AIDS. In spite of the similarities between FIV and HIV, there is no evidence that FIV is a health hazard to man or other species of animals.